Insulin-dependent diabetes mellitus (IDDM), also known as type I diabetes, is characterized by reduced insulin production and hyperglycemia, i.e., high blood glucose levels, which ultimately results in a variety of early symptoms in humans, including increased thirst, frequent urination, extreme hunger, unintended weight loss, fatigue and blurred vision. Untreated, IDDM can ultimately lead to tissue damage, resulting in increased risk of heart attacks and strokes, neuropathy, retinopathy, kidney failure and, ultimately, death. IDDM is one of the most prevalent metabolic disorders in the world. In the United States, approximately one in 300 to 400 people are affected by this disease. Some studies suggest that the incidence of IDDM in the United States is continuing to rise.
Different therapies have been employed for treating IDDM. By far the most commonly employed therapy for the clinical symptoms of IDDM is exogenous insulin replacement. However, while insulin replacement therapy allows most IDDM patients to lead somewhat normal lives, this therapy is imperfect and does not completely restore metabolic homeostasis. As a result, severe complications including dysfunctions of the eye, kidney, heart, and other organs are common in diabetic patients undergoing insulin replacement therapy. See U.S. Pat. No. 6,207,159, which is hereby incorporated by reference in its entirety.
Another common treatment for the clinical symptoms of IDDM is pancreatic or beta-islet cell transplantation. However, the insulin-producing beta-cells of transplanted tissues are often rapidly destroyed by the same autoimmune response which previously destroyed the patient's own pancreatic tissue. Therefore, the use of immune-suppressants after transplantation is common, carrying with it the adverse side effects described above. See U.S. Pat. No. 6,207,159, which is hereby incorporated by reference in its entirety.
There remains a need for improved treatments of IDDM. The present invention addresses this need.